Purpose of review: This article presents an overview of the most recent and important strategies to reduce secondary brain damage.
Recent finding: There is currently no magic bullet available to protect the brain after neuronal injury. This is related to the complex pathophysiology of cerebral ischemia, which makes it unlikely that a single pharmacological intervention results in sustained neuroprotection. Analyses of clinical studies reveal that acute physiologic derangements (e.g. fever, hypertension and hypotension, hypoxemia, hypercapnia, hyperglycemia) are the most important predictors of unfavorable outcome after brain injury and have to be treated. The effectiveness of anesthetic agents to extend the ischemic tolerance of neurons has been demonstrated in experimental settings, but such benefits have not been demonstrated in humans. The effectiveness of osmodiuretics to decrease elevated intracranial pressure, a factor with relevance to outcome, has been demonstrated. Infusion of magnesium in patients with subarachnoidal hemorrhage can reduce the occurrence of delayed ischemia caused by cerebrovascular spasm. The prophylactic administration of glucocorticoids should be avoided. While the positive effects of chronic administration of statins to reduce the incidence of stroke has been demonstrated in several clinical studies, the protective effect of acute administration of statins after a cerebral insult has do be defined.
Summary: Control of physiological variables, avoidance of hyperthermia, intensive control of plasma glucose concentrations, use of anesthetic agents and osmodiuretics to control intracranial hypertension and the possible prophylactic administration of magnesium in patients at risk of vasospasm and of statins in patients with cerebrovascular risk factors are currently the most important strategies to reduce neuronal injury.